The destructive lung disorders are diseases in which there is a desolution and loss of alveolar structures. The primary mechanism responsible for this is an imbalance of proteases and antiproteases toward proteases, particularly neutrophil elastase. Studies of patients with hereditary PiZ homozygous Alpha 1-antitrypsin deficiency demonstrated that they have neutrophils in their lungs, active neutrophil elastase and very little Alpha-1 antitrypsin. Intraveneous therapy with partially purified Alpha 1-antitrypsin to these individuals demonstrate not only is the antielastase screen of the lower respiratory tract restored but the active elastase is removed. Although there are some patients with this hereditary disorder that do not have emphysema, the primary determinant of disease appears to be the presence of neutrophils in the lung as well as the neutrophil proteolytic enzymes. Therapy with Danazol, and impeded androgen, has shown that serum Alpha 1-antitrypsin levels can be maintained 50 percent above baseline levels for extended periods of time without complications.